title: Markers of inflammation, endothelial activation, and arterial stiffness in hypertensive heart disease and the effects of treatment: results from the SILVHIA study.
abstract: We assessed the contribution of blood pressure (BP), inflammation, and endothelial activation to the development of structural vascular and cardiac changes in hypertension. Furthermore, the effects of antihypertensive therapy were studied. We studied 114 patients with hypertension and left ventricular hypertrophy and 38 matched hypertensive subjects without cardiac hypertrophy and 38 normotensive subjects. The group with hypertension and cardiac hypertrophy were randomized to treatment with an angiotensin receptor blocker (irbesartan) or a beta-adrenergic receptor blocker (atenolol) for 48 weeks. Markers of inflammation (high-sensitive C-reactive protein, interleukin-6, leukocyte counts), vascular function (ambulatory aortic stiffness index, arterial compliance, and pulse pressure), and endothelial activation (E-selectin, intracellular adhesion molecule-1, vascular adhesion molecule-1) were assessed. Markers of inflammation and arterial stiffness were lowest in the normotensive group and highest in patients with hypertensive heart disease; endothelial markers were similar between groups. Inflammation was independently related to BP. Markers of arterial stiffness were independently related to BP and to a lesser extent to left ventricular mass. Antihypertensive treatment improved arterial compliance; inflammatory and endothelial markers remained unchanged. In conclusion, markers of inflammation and arterial stiffness are independently related to BP. Antihypertensive therapy seems to improve arterial stiffness, but effects on markers of inflammation and endothelial activation are small.
authors.affiliation: Division of Cardiovascular Medicine, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden. D. Mörtsell is now with the Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
authors.forename: Andreas
authors.initials: A
authors.lastname: Jekell
authors.forename: Karin
authors.initials: K
authors.lastname: Malmqvist
authors.forename: N Håkan
authors.initials: NH
authors.lastname: Wallén
authors.forename: David
authors.initials: D
authors.lastname: Mörtsell
authors.forename: Thomas
authors.initials: T
authors.lastname: Kahan
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001158:Arteries / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology; D001262:Atenolol / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D001713:Biphenyl Compounds / Q000627:therapeutic use; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood* / Q000378:metabolism; D000077405:Irbesartan; D008297:Male; D008875:Middle Aged; D013777:Tetrazoles / Q000627:therapeutic use; D014655:Vascular Resistance / Q000187:drug effects; D059289:Vascular Stiffness / Q000187:drug effects*
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D015415:Biomarkers; D001713:Biphenyl Compounds; D018836:Inflammation Mediators; D013777:Tetrazoles; D001262:Atenolol; D000077405:Irbesartan